the rectal temperature peak (112.0°F) but the blood pressure fluctuated jerkily from 

 66.0 mm. Hg. to 90.0 mm. Hg. then from 76.0 mm. Hg. to 90.0 mm. Hg, at body tempera- 

 ture 111.2°F followed by a rapid fall to 34.0 mm. Hg. and with recovery to 66.0 mm. 

 Hg. at the conclusion of the cooling treatment. This rabbit responded to a rising 

 body temperature by increase of respiratory activities, ventilation being adequate 

 for the carbon dioxide levels in expirations until the body temperature 111.8°F was 

 attained. At this point there was respiratory failure, characterized by unresponsive- 

 ness of the respiratory centre at the body temperature peak and progressive deterior- 

 ation during the cooling treatment, there being no sign of stimulatory response for 

 the respiration during this phase. The blood pressure, however, responded favour- 

 ably, at the conclusion of cooling treatment. 



It may be significant that the circulation appeared to be favourably influenced 

 by cooling treatment to which the respiration was unresponsive. There was no ap- 

 parent addition of fluid to the intra- vascular system during the phase of heating up; 

 and there appeared to be progressive loss of fluid from the circulation after the body 

 temperature 107 .8°F continuing steadily up to the peak of body temperature; haemo- 

 globin rise 19%. At the conclusion of the acute experiment, the rabbit was rather 

 dazed, but otherwise seemed in good condition. Examined at 9.30p.m. that day she 

 was found lying on her side, unable to stand or walk, breathing rapidly, heart rate 240 

 beats per minute, sounds quiet but audible. The rectal temperature was 88.6-°F (sub- 

 normal) the room temperature at this time was 96.8°F. The blood pressure was too 

 low to record. While we were attempting to obtain blood for a haemoglobin estima- 

 tion, the rabbit gave a number of violent inco- ordinate movements and died at 

 9.40p.m. At autopsy, performed immediately, the limbs and abdominal muscles were 

 very stiff, heart contracted and hard, petechial haemorrhages in the walls of the 

 small intestine, bladder distended with brownish fluid, ears very white, suprarenals 

 very pale in colour, abdominal viscera deeply engorged, fluid in the peritoneal 

 cavity under pressure, limb muscle white. The death of this rabbit appeared to be 

 due to some form of peripheral circulatory failure, emphasis being probably on 

 capillary damage rather than failure of the heart or vasomotor centres, except per- 

 haps as a secondary effect. The associated poikilothermia, however, may have been 

 due to damage to the controlling centres, since the respiratory centre became unres- 

 ponsive after the exposure, and showed no sign of improvement during cooling; even 

 though the blood supply to the respiratory centre — judging from the recorded blood 

 pressure — should have been adequate, in the absence of spasm of the cerebral 

 arteries and arterioles. (This suggestion is at variance with physiological dogma, 

 but we have several instances where the only explanation for central failure seemed 

 to be spasm of the cerebral arteries or arterioles.) 



Our time is getting short, and I have outlined some of the problems involved in 

 the effective treatment of cases of heat stroke. Rapid cooling of the whole body 

 was the best treatment for the hyperthermic crisis; the delayed collapse in cases 

 successfully cooled was combated in a number of ways; very useful was an extract 

 of the cortex of the suprarenal gland, injected subcutaneously. The associated 

 damage to the central nervous system was investigated; we found focal ischaemic 

 areas scattered throughout the cerebral hemispheres, the cerebellum, and in some 



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